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Topic: Yale University study on Alzheimer's and Immune System (Read 3674 times)

Alzheimer’s research at Yale University has concluded that immune cells can be enticed into the brain to destroy amyloid plaques associated with Alzheimer’s. In the Yale research project they used double-trangenic Alzheimer’s mice which performed beyond expectation through the mazes. The reason? Because the improved immune systems of the mice in the study had caused the reduction of the amyloid in the brain by up to 90%.

The Yale University research seems to support the two Alzheimer’s papers of The Endowment for Medical Research published from our Nutritional Pilot Surveys where we were able to activate the macrophages and improve the human immune system with what I call in my book, ROYAL SUGARS.

Some doctors are now finding Alzheimer’s patients are performing beyond expectation through the maze of brain function challenges because of improved immune function. The reason for improved brain function is probably the reduction of amyloid plaque build-up on the neurons.

To many, the maze is less confusing than before. A modest grant could help us evaluate what we have actually done which should be relatively easy to accomplish through reverse engineering.

The pharmaceutical companies are scrabbling through mazes while throwing billions of dollars into new drug development to treat the symptoms of diseases. Glycomics can and will be integrated into main stream medicine over the next twenty years.

Meanwhile, the general public does not want to wait and they may not have to. The cheese in the box is on the far side of the maze. The sugars are outside the box of normal healthcare. If we are going to cut the OUT OF CONTROL costs of healthcare, we are going to have to think outside the box.

And now, the article about the discovery at Yale University.

Immune cells 'vacuum up' Alzheimer's clumps

Debris-gobbling immune cells can be enticed into the brain to eat away the amyloid plaques associated with Alzheimer's disease, according to a study in mice.

The study suggests a promising new approach in the fight against Alzheimer's – and several drug candidates are already on pharmaceutical company shelves, waiting to be tried out.

Richard Flavell at Yale University in New Haven, Connecticut, and his colleagues created a double transgenic mouse, dubbed Tg2576-CD11c-DNR. One gene predisposed it to develop amyloid plaques in its brain that mimic Alzheimer's disease, while another blocked the activity of TGF-beta, a cytokine.

The researchers had expected the double-transgenic mice to do even more poorly than their single-transgenic Alzheimer's cagemates. But as the animals got to old age – about 18 months – the Tg2576-CD11c-DNR mice performed significantly better at traversing through various mazes. When the researchers examined their brains, they found up to 90% less amyloid.

For reasons that are not entirely clear, selectively blocking TGF-beta allowed macrophages, immune cells that ingest unwanted materials, to get across the blood brain barrier and into the brain. There, they feasted on amyloid plaques. "It was like a vacuum cleaner," says Flavell.

Several drug candidates already exist that are known to block TGF-beta in a similar way. It's too early to know if such a drug would be able to roll back the symptoms. "But even to reverse the decline would be an improvement," says Flavell.